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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RA9xViiguELAs7QEhDCoYcF1GJciS2ASx5W32JLmTYKdE#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RA9xViiguELAs7QEhDCoYcF1GJciS2ASx5W32JLmTYKdE#_5 http://www.w3.org/ns/prov#value Since HO-1 gene expression is strongly induced by agents or conditions that increase oxidative stress, redox signaling plays a crucial role in its regulation. These stimuli include heavy metals, bacterial lipopolysaccharides, hypoxia, hyperoxia, heat shock, ischemia, UV radiation, H2O2, cytokines, nitric oxide, stimuli that deplete cellular glutathione stores, and its substrate heme (Applegate et al., 1991; Shibahara, 1994; Immenschuh and Ramadori, 2000). In addition, several different redox-independent signaling pathways are involved in HO-1 gene regulation (Immenschuh and Ramadori, 2000). 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